The measurements of renal NAE and urine pH values unequivocally confirmed that diet composition can significantly influence acid-base metabolism: consumption of a lactovegetarian diet (LP) results in only minute differences between the non-bicarbonate anion excretion on the one hand and the mineral cation excretion on the other [ı (Cl + P04 + SO4 + OA - Na - K - Ca - Mg) < 10 mEq; Table 3], thus minimizing the necessity for a compensatory increase of renal proton (Hı, TA, NH4) excretion. Obviously, the opposite is the case after ingestion of a high-protein diet providing low amounts of fruits and vegetables. For such a diet the sum of the urinary nonbicarbonate anions can exceed the sum of the mineral cations by > 100 mEq, leading to a corresponding increase in NAE.
A usual Western diet with a moderately high protein content (similar to MP) induces an acid excess of ı 50- 100 mEq/d (9, 24), intermediate between a lactovegetarian and a highprotein diet. The NAE concentration found for the MP diet corresponds well with the literature data. According to Robertson and Peacock (24) the overall urinary pH is dependent on the composition of the diet: the higher the protein content of a diet, the lower the urinary pH. Whether such a clear relationship between diet composition and urinary pH does actually exist in the case of shifting from a vegetarian to an omnivorous diet (or vice versa), has been questioned by other authors (8). The present data, however, provide clear evidence that dietetic measures leading to lactovegetarian nutrition can significantly increase urinary pH (MP vs LP, P < 0.01). In addition, through the mere ingestion of a diet characterized by high protein content but only minute amounts of plant foods, comparably low urinary pH values can be achieved as for administration of the strongly urine-acidifying amino acid L-methionine, taken with a normal diet. Thus, a urinary pH adjustment to ı 5.5 is attainable by purely dietetic measures. This could be of practical relevance, eg, for the prevention of calcium-phosphate stone precipitation (in individuals at risk).
The low pH reached on HP (as well as on MP + methionine) was very near the urine pH area of maximum stimulation of renal acid excretion characterized by urinary pH values falling below 5.4 (25). This indicates that there was not more much functional reserve left for getting rid of further acid loads. In consequence, the ingestion of very high amounts of protein concomitantly with little food of plant origin bears a risk for the development of metabolic acidosis. Attention should be paid to this, especially when extremely protein-rich diet regimens (eg, for bodybuilders and weight lifters) are composed. Such diets should provide adequate amounts of alkalizing constituents, ie, enough fruit and vegetables.
On the other hand, when protein intake is strongly reduced concomitantly with a marked increase in the consumption of fruit and vegetables, urinary pH values of 6.6-6.8 can be achieved (Table 3) as is recommended for the therapy of uric acid lithiasis (Uric Acid Stones) (26).
As shown in Table 3 the urinary excretion rates of individual minerals (except for calcium) were estimated with a relatively low estimation error. The discrepancy between measured and estimated excretion rates of calcium especially seen with the LP and MP diets can be, at least partly, explained by findings showing that increased intakes of protein and/or acid can augment urinary calcium losses (27). The regression equation used in our calculation model for the estimation of renal calcium excretion rates from calcium intake data takes no account of the reduction in renal calcium losses due to decreased protein intake or decreased acid load.
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See also
A High Ratio of Dietary Animal to Vegetable Protein Increases the Rate of Bone Loss and the Risk of Fracture in Postmenopausal Women